The present invention relates generally to implantable medical devices. Many embodiments of the invention are directed more particularly to monitoring acute, episodic, or chronic cardiac dysfunction conditions, including heart failure (HF), and/or treating such conditions by providing appropriate therapies.
Congestive heart failure is an extremely serious affliction. Heart failure (HF) is not a specific disease, but rather a compilation of signs and symptoms, all of which are caused by an inability of the heart to appropriately increase cardiac output during exertion. HF may be caused by chronic hypertension, ischemia, tachyarrhythmias, infarct or idiopathic cardiomyopathy. HF has a great impact on the quality of life, as the sympathetic nervous system is placed in a state of hyperexcitablity, leading to a loss of heart rate variability and rate responsive mechanisms in the heart. In turn, the ability of the heart to relax is impaired, resulting in elevated filling pressures, pulmonary congestion, and low exercise tolerance. These are just a few of the side effects.
The treatment of severe cardiac dysfunction and decompensated heart failure may include inotropic drug therapies. Although these therapies may be beneficial in specific settings, they require administration of a drug, often by intravenous route, with systemic side effects and the time-consuming involvement of skilled clinicians. Electrical stimulation therapies are attractive alternatives because implanted or external devices may administer them very shortly after dysfunction appears or worsens and because their actions may be confined to the heart.
Delivering stimulation during the refractory period of the cardiac cycle is a type of therapy generally referred to as increased cardiac contractility (ICC). ICC therapy, used in this manner, has been observed to cause release of catecholamines such as norepinephrine within the tissue of the heart, potentially contributing to an observed increase in contractility of the cardiac tissue, which in turn, results in increased cardiac output, fewer symptoms of heart failure, and improved exertional capacity. Such ICC therapy may also alter calcium influx from the intra-cellular space into the cardiac myocyte, which could increase the amount of calcium available for muscles contraction both directly and through greater SR calcium uptake and subsequent release.
Another type of electrical stimulation can be provided during the nonrefractory period of the cardiac cycle to enhance cardiac function. This type of paired and coupled stimulation of heart tissue results in an additional electrical depolarization and, when appropriately timed, results in post extrasystolic potentiation (PESP). The additional depolarization, coming shortly after a first depolarization, is likely not associated with a sizable mechanical contraction, and results in increased contractility of subsequent cardiac cycles.
As is known, the above-described therapies, ICC and PESP, as well as other therapies, including pacing, cardiac resynchronization therapy (CRT), and defibrillation capability, may be used alone or in certain combinations to treat cardiac dysfunction, including HF. However, designers of prior art systems utilizing such therapies have needed to proceed with caution in order to provide systems that are both safe and effective. Specifically, regimens have been designed to provide one or more of the therapies in a manner that is most beneficial without significant risk of initiating potential arrhythmia. Delivery of electrical stimulation as the heart tissue is becoming non-refractory can trigger a tachyarrhythmia. This is particularly true if multiple high-amplitude pacing pulses are utilized. Therefore, becoming familiar with appropriate timing parameters associated with one or more of these types of therapies has been essential.
What is needed are additional systems and/or methods that utilize the one or more known therapies available for treating cardiac dysfunction, including HF, in manners that further optimize mechanical function or cardiac output, while also further minimizing the limitations of known cardiac dysfunction therapies.